Recent attention has focused on the untoward effects of prenatal cocaine exposure on a child's health and development. The most alarming outcomes relate to abnormal neurodevelopmental findings, increased respiratory pattern abnormalities, and the reported but controversial increased incidence of Sudden Infant Death Syndrome (SIDS). These studies are based on the general assumptions that 1) in utero cocaine exposure disrupts CNS maturation particularly in areas of wakefulness and sleep, and that 2) the manifestations are evident even prior to birth. Assuming that central arousal mechanisms are altered by in utero cocaine exposure, we suggest that the functional markers of this CNS injury will be manifested in the human fetus and infant as altered state differentiation, integration, and regulation and in altered respiratory control. Postnatal state development will be evaluated behaviorally and by 10- hour overnight polysomnographic recordings for sleep architecture and occurrence of short arousals (defined by behavioral, physiologic, and EEG criteria). Respiratory pattern abnormalities during sleep states will be assessed by evaluating the presence of apnea (central, obstructive, mixed) and periodic breathing with and without desaturations; hypoxic arousal and hypercarbic ventilatory tests will also be administered. The extent of cardiorespiratory interactions will be examined by estimates of respiratory variation of heart rate. Mothers will be enrolled prenatally and the mother-child pairs followed to the child's 6th month. Infant and maternal charts will be reviewed for medical complications that could also influence outcome measures. Biological markers of prenatal exposure will be determined by maternal and newborn urine screens and by newborn meconium screens. Intake and subsequent serial interviews will assess known biological and caregiving confounds of cocaine use as well as add to our ability to address pattern and timing of cocaine use. These studies will increase our understanding of prenatal cocaine effects on respiration and state development. A benefit from these studies may be identification of early fetal and neonatal markers of risk making possible early interventions for these and other high risk infants. The SIDS Risk Study has completed year two of a four year award. Three groups of women/infant pairs are recruited. Group classification is blind to the investigators. Coding has not been broken nor data obtained from the polysomnography, pulmonary or developmental studies performed in the GCRC. However, preliminary data from the fetal component have been analyzed. Early prenatal data suggest group differences in prenatal state development and state regulation. Alterations in state and state regulation suggest attentional deficits found even prior to birth and implicate specific neurodevelopmental effects of cocaine and nicotine exposure. These data may have important clinical implications for early identification of infants at risk for SIDS.